Used Kruskal-Wallis and Mann-Whitney U tests to statistically analyse the eachUsed Kruskal-Wallis and Mann-Whitney U

Used Kruskal-Wallis and Mann-Whitney U tests to statistically analyse the each
Used Kruskal-Wallis and Mann-Whitney U tests to statistically analyse the each group mutually. We stated the histopathological and histochemical results as the median (min-max) where p < 0.05 was found statistically significant.oli and pulmonary edema. Where these findings represent a pulmonary edema, the extravasation of fluid is the most common finding in histophatological examination. The results of this histopathological examination are presented in table 1. The most noticeable finding is real reexpantion pulmonary edema and it occurred in only two animals in the RPEG group. The severity of the pulmonary edema was significantly reduced in the Taurine administrated group. Real reexpantion pulmonary edema's characterization includes severe pulmonary edema with PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28607003 alveolar damage and acute inflammation. Various severity levels of reexpantion pulmonary edema are shown at the figure 2. In RPEG group animals, accumulations of alveolar macrophages with sparse neutrophilic infiltrate at the alveolar and interstitial edema regions are indicated.MDA levels, GPx and SOD activities in tissue Oxidative stress status analysis included MDA level, SOD and GPx activity. RPE caused increased MDA levels, and decreased GPx and SOD activity significantly in lung tissue (P < 0.05) (Table 2). Taurine treatment decreased MDA levels and increased SOD and GPx activities compared with RPEG (P < 0.05). MDA in RPEG was much higher than that in TG (P < 0.05). In addition, SOD and GPx activities in TG were approximately as same as activities of those in Group CG (P > 0.05).DiscussionThere are some studies about reinflation of a collapsed lung can lead to pulmonary edema of the reexpanded lung [5]. RPE has a mortality rate changing from 0 to 20 [3,13]. Some of the patients’ conditions who had severe RPE further deteriorated leading to bradycardia, hypotension, cardiopulmonary arrest and death [4]. There are some studies about causes of RPE [2]. It is emphasized that the most important reason of RPE is the prolonged collapse of a lung for 72 hours before PF-04418948 msds reexpancion [2]. In the light of these knowledge, in our study, we kept the lungs collapsed for 72 hours to develop RPE. ReTable 1: Histopathology results of the groups.CG n Normal Pulmonary Parenchyma Fluid Extravasations Fluid Extravasations with Fluid In The Alveoli Real reexpancion Pulmonary Edema 10 10 0 0RPEG 10 0 2 6TG 10 4, 4 2ResultsHistopathological evaluation The final results of the performed histophatological examination were; normal pulmonary parenchyma, fluid extravasations, fluid extravasations with fluid in the alve-CG; Control Group, RPEG; Re-expansion Pulmonary Edema Group, TG; Taurine Treatment Group. : p < 0,05, RPEG compared with CG; : p < 0,05, TG compared with RPEG, : p < 0,05, TG compared with CG.Page 3 of(page number not for citation purposes)Journal of Cardiothoracic Surgery 2008, 3:http://www.cardiothoracicsurgery.org/content/3/1/Figure 2 (c) Severe pulmonary edema with alveolar damage and typical acute accumulation in in RPEof the RPE (HEx400), (d) Fluid extravasationedema perivascular areas, (HEx200), (b) Esinophilic fluid inflamatory cells some cells in alveolar spaces (HEx100), (a) Severe pulmonary in the with alveolar damage and scattered scattered typical acute inflamatory (HEx200) (a) fluid extravasation in the perivascular areas, (HEx200), (b) esinophilic fluid accumulation in some of the alveolar spaces (HEx100), (c) severe pulmonary edema with alveolar damage and scattered typi.